Porokeratosis
☆ Mune 2022 Stiftung Warentest mhedzisiro kubva kuGermany, kugutsikana kwevatengi neModelDerm kwakangodzikira zvishoma pane nekubhadharwa kwe telemedicine kubvunzana.
Iwo akaomerwa mapendekete akabudikira ane hunhu.
References
Porokeratosis chiitiko cheganda chisingawanikwe chinoratidzwa nezvinetso zvekeratinization, zvichikonzera kukwidziridzwa, zvigamba zvakaita semhete kana mabumbu akakasharara paganda. Chinhu chayo chinotsanangura pasi pe microscope kuvepo kwe cornoid lamella, kurongeka kwemasero ari pamusoro peganda. Porokeratosis inouya nenzira dzakasiyana siyana (disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, linear porokeratosis) . Zvakakosha kuziva kuti porokeratosis inogona kuita gomarara reganda. Nzira yakanakisa yekuongorora porokeratosis ndeye biopsy yemuganho wakasimudzwa, kunyangwe parizvino hapana chiyero chekurapa.
Porokeratosis is an uncommon dermatologic disorder. It is a disorder of keratinization that presents with keratotic papules or annular plaques with an elevated border. It has a distinct histologic hallmark of cornoid lamella, which is a column of tightly fitted parakeratotic cells in the upper epidermis. There are multiple clinical variants of porokeratosis, including disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, and linear porokeratosis. Porokeratosis is a precancerous lesion that can undergo malignant transformation. Evaluation of porokeratosis is best with a biopsy of the elevated border. There are no standard guidelines for treatment.
Porokeratosis is an uncommon dermatologic disorder. It is a disorder of keratinization that presents with keratotic papules or annular plaques with an elevated border. It has a distinct histologic hallmark of cornoid lamella, which is a column of tightly fitted parakeratotic cells in the upper epidermis. There are multiple clinical variants of porokeratosis, including disseminated superficial actinic porokeratosis, classical porokeratosis of Mibelli, porokeratosis palmaris plantaris et disseminatum, and linear porokeratosis. Porokeratosis is a precancerous lesion that can undergo malignant transformation. Evaluation of porokeratosis is best with a biopsy of the elevated border. There are no standard guidelines for treatment.
Disseminated superficial actinic porokeratosis (DSAP) chirwere chekuvhiringidzika keratinization. Ndiyo imwe yemhando nhanhatu dzeporokeratosis, uye inowanzobata nzvimbo dzakakura zvichienzaniswa nedzimwe (linear, Mibelli's, punctate, palmoplantar disseminated, superficial porokeratosis) . Mhando inoputika ye porokeratosis inowanzobatana nekenza, kushaya simba kwekuzvidzivirira, kana kuzvimba. Zvinhu zvine njodzi zvinosanganisira genetics, kudzvanywa kwe immune, uye kuratidzwa nezuva. DSAP inotanga semapundu epingi kana shava ane mipendero yakasimudzwa munzvimbo dzine zuva, dzimwe nguva zvichikonzera kuvaviwa zvishoma. Mishonga inosiyana uye inogona kusanganisira topical creams, light therapy, kana mishonga yakaita se5-fluorouracil kana retinoids. Maronda aya anonzi precancerous, aine 7. 5 - 10 % mukana wekushanduka kuita squamous cell kana basal cell carcinoma.
Disseminated superficial actinic porokeratosis (DSAP) is a disease of disordered keratinization. Disseminated superficial actinic porokeratosis is one of six variants of porokeratosis. It has more extensive involvement than most other variants. These other variants include linear porokeratosis, porokeratosis of Mibelli, punctate porokeratosis, porokeratosis palmaris et plantaris disseminata, and disseminated superficial porokeratosis. The eruptive form of porokeratosis is associated with malignancy, immunosuppression, and a proinflammatory state. Risk factors for porokeratosis include genetics, immunosuppression, and ultraviolet light. The lesions in disseminated superficial actinic porokeratosis start as pink to brown papules and macules with a raised border in sun-exposed areas that can be asymptomatic or slightly pruritic. There are many options for the treatment of disseminated superficial actinic porokeratosis, including topical diclofenac, photodynamic therapy (PDT), 5-fluorouracil (5-FU), imiquimod, vitamin D analogs, retinoids, and lasers. These lesions are considered precancerous. There is a 7.5 to 10% risk of malignant transformation to squamous cell carcinoma or basal cell carcinoma.
Disseminated superficial actinic porokeratosis (DSAP) is a disease of disordered keratinization. Disseminated superficial actinic porokeratosis is one of six variants of porokeratosis. It has more extensive involvement than most other variants. These other variants include linear porokeratosis, porokeratosis of Mibelli, punctate porokeratosis, porokeratosis palmaris et plantaris disseminata, and disseminated superficial porokeratosis. The eruptive form of porokeratosis is associated with malignancy, immunosuppression, and a proinflammatory state. Risk factors for porokeratosis include genetics, immunosuppression, and ultraviolet light. The lesions in disseminated superficial actinic porokeratosis start as pink to brown papules and macules with a raised border in sun-exposed areas that can be asymptomatic or slightly pruritic. There are many options for the treatment of disseminated superficial actinic porokeratosis, including topical diclofenac, photodynamic therapy (PDT), 5-fluorouracil (5-FU), imiquimod, vitamin D analogs, retinoids, and lasers. These lesions are considered precancerous. There is a 7.5 to 10% risk of malignant transformation to squamous cell carcinoma or basal cell carcinoma.
Mumwe murume ane makore 52 okukura, aimbova noutano hwakanaka, akauya aine chigamba chakati sandara, chakaita serin’i pamucheto wechigunwe chechina, icho chakanga chavepo kwemakore maviri pasina kukonzera zviratidzo. Yakatanga idiki, yakaoma bundu uye yakakura kunze nekufamba kwenguva. Kunyangwe kuedza kurapwa kwakasiyana senge cryotherapy, makirimu, antifungals, uye mishonga inorwisa mabhakitiriya, chigamba chacho hachina kuita nani. Kunyatsoiongorora nedermocopsy yakaratidza pakati pakaoma, dzvuku nemuganhu wakakora, wakaoma. Chidimbu chidiki cheganda chakatorwa kubva kumucheto kwechigamba chakaratidza kukura kwesero rekunze mukati meganda, zvichisimbisa kuongororwa kwe porokeratosis of Mibelli.
A 52-year-old man with no past medical history presented with an asymptomatic annular atrophic patch on the distal portion of the fourth toe of 2 years’ duration. The lesion began as a small keratotic papule that gradually enlarged centrifugally. He had received multiple treatments including cryotherapy, topical corticosteroids, antifungals, and antibiotics without improvement. Dermoscopic examination revealed a scaly atrophic erythematous central area with a sharply demarcated peripheral hyperkeratotic structure. A skin biopsy of the edge of the lesion revealed a cornoid lamella with a column of parakeratotic cells extending from an invagination of the epidermis with absence of granular layer. The clinicopathologic correlation was consistent with porokeratosis of Mibelli.
A 52-year-old man with no past medical history presented with an asymptomatic annular atrophic patch on the distal portion of the fourth toe of 2 years’ duration. The lesion began as a small keratotic papule that gradually enlarged centrifugally. He had received multiple treatments including cryotherapy, topical corticosteroids, antifungals, and antibiotics without improvement. Dermoscopic examination revealed a scaly atrophic erythematous central area with a sharply demarcated peripheral hyperkeratotic structure. A skin biopsy of the edge of the lesion revealed a cornoid lamella with a column of parakeratotic cells extending from an invagination of the epidermis with absence of granular layer. The clinicopathologic correlation was consistent with porokeratosis of Mibelli.
Kazhinji biopsy inoitwa nekuti inogona kutaridzika yakafanana neactinic keratosis kana squamous cell carcinoma.